by Jonathan Lee, MD

Pelvic structures are held together by the strong ligamentous connections surrounding it; this is disrupted in pelvic fractures. Keep in mind that the internal iliac vessels and the lumbosacral plexus are intimately associated with posterior pelvic ligaments.

MORTALITY RATE 15-25% for closed fractures, as much as 50% for open fractures… most commonly caused by hemorrhage. The pelvis can hold up to 3-4 liters of blood (nearly HALF your body’s blood volume!)

ASSESSING THE PELVIS

Inspection for ECCHYMOSIS; it can point you towards a bleeding pelvic fracture:

Periumbilical (Cullens Sign)

Flanks (Grey Turner Sign)

Iguinum / Perineum / Scrotum / Upper Thigh (Destot Sign)

Check for GROSS HEMATURIA – 21% of males and 8% of females.

Check the vagina and rectum to rule out OCCULT OPEN FRACTURES … if so: abx are imperative.

Apply gentle rotational force on each iliac crest

PERFORM THIS ONLY ONCE! DO NOT ‘ROCK’ THE PELVIS!

low sensitivity for detecting instability Get a bedside pelvic x-ray

MANAGEMENT

RESUSCITATION – CABDE (worry about those catastrophic bleeds).

Consider massive transfusion!

PRBC:FFP:Platelets ideally should be transfused 1:1:1

PELVIC BINDER

The purpose of a pelvic binder is to CONTROL BLEEDING. It should be centered over the GREATER TROCHANTERS. Do not place over iliac crest/abdomen. Augment with internal rotation of lower extremities and taping at ankles/knees.

CLASSIFICATION

The most commonly used system is the young-burgess system that organizes fractures by direction of the impact force:

Anterior-Posterior compression

Lateral compression

Vertical Sheering

So when you check your pelvis x-ray, quickly MEASURE to see if there is >2.5cm displacement of the symphysis pubis and >1cm displacement between he sacroiliac joints! This may not only point you towards disposition (surgery vs. conservative management) but also indicates to what degree of bleeding to expect. More displacement = More sheering of vessels.

Keep in mind that 80-90% of pelvic fracture bleeds are venous. Yes, they may be brisk bleeds that present to your trauma room hypotensive, but they can also be slow bleeds. So if your patient stays in your ER longer than intended, make sure you get serial H/H’s.

by Jonathan Lee, MD

Total five species (Zaire to have the highest mortality – named after the country in which it was first discovered)

Category A Bioterrorism Agent – Agents with High transmission/dissemination and high mortality – along with Small Pox and the Bubonic Plague.

Discovered in Zaire (or current day Democratic Republic of Congo) in 1976. Named after a tributary that branches off of the Congo River that was near the site of initial outbreak.

Since 1976, there have been 14 outbreaks of Ebola Virus (including current). All have been in either in Zaire/DRC, Gabon, or Sudan.

Pathogenesis

Unclear however likely secondary to animal vector. Original host thought to be bats as they have frequently been isolated to carry the virus without actually being affected. Likely bat drops a piece of partially eaten fruit, drops it on the ground, which then other animals consume humans hunt for bushmeat…

Transmission

Body fluid contact with either open skin or contact with any mucosa. Can be carried in serum, tears, urine, saliva, semen, vaginal fluids. Thought to last in sperm even post infection. Infections go up once patients get admitted to hospitals secondary to close contact. Proper personal protective equipment and hygiene is paramount to preventing spread.

Pathophysiology

Virus can invade any cell in the body however preferentially attacks three:

Neutrophil CD16B – Suppresses your immune system initially.

Endothelium – Leading to hemorrhage. Inflammation can also trigger DIC.

by Elizabeth Perry, MD

35 yo F presents to your Resus Room. She’s hypotensive, and not really responding to fluids, and have tried almost all of your pressors. You find out from her accompanying family members that she’s an asthmatic, steroid dependent, and hasn’t been able to make her insurance payments on time as of recent.

Primary Adrenal Gland Insufficiency = Addison’s
-destruction of > 90% of adrenal glands
-Results in decreased cortisol and aldosterone production
-rare
-causes: autoimmune destruction, hemorrhage (from use of warfarin,sepsis, trauma), tumor (breast and melanoma), infection (HIV, Tb, meningococcemia) or inflammatory process.
-In US 70% of primary AI is due to autoimmune disorders. Can be isolated or associated with polyglanduar autoimmune syndrome (PGA) type I or II.
–About 20% of HIV patients eventually develop adrenal insufficiency, most common infectious cause in US. Worldwide most common infectious cause is TB.

Secondary Adrenal Gland Insufficiency
-insufficient production of ACTH. Occurs following disorders in the hypothalamic–pituitary axis, when CRF and/or ACTH fails to be secreted.
–most common cause is suppression of HPA axis over time due to long term therapy with pharmacologic doses of glucocorticoids.
-other causes: destruction or dysfunction of the pituitary (pituitary disease, head trauma, postpartum pituitary necrosis- Sheehan Syndrome)
-mineralocorticoid (aldosterone) function intact, loss of glucocorticoid (cortisol) activity

by Stephen Strasberg, MD

Handoff = Signout = Dangerous

It is well known that patient handoffs are a dangerous time for patients. Information is exchanged and whenever this happens, inevitably something gets lost in the mix.

What can you do to help your patients? Have a system. Any system really, but just having a system in place to signout or handoff patients in a systematic way will reduce medical errors and keep your patients safer. There are numerous systems out there. JCAHO and WHO use SBAR. Our friends and UNM (University New Mexico) use PLAN ED. Here is their policy.

“Run the List” (go over next steps for all patients so that a clear plan is presented at handoff) within the hour leading up to the shift change with the attending.

Reevaluate high-risk patients (patients who have already been handed off once and/or who do not have a clear diagnosis or disposition plan) within the hour leading up to handoff.

Write down key lab values for acutely ill and complicated patients within thirty minutes of handoff. Time permitting, radiology findings and current vital signs should also be included.

Handoff Presentation

All providers should use the same structured format for handoff presentations in order to facilitate the consistency and completeness of communication among providers and nursing staff.

Everything else (social issues, handed off before, systems issues)

Disposition

Be on time and prepare for handoff early so that handoffs can start when scheduled

Organize handoffs by doing selected “bedside waking rounds”

Proven Techniques for Effective Handoffs

Incorporate the use of written notes and/or electronic medical records (EMR) in handoff (has been proven to reduce physical exam and lab result memory errors, especially for patients who have been in the ED for prolonged periods of time)

Officially admitted patients (have bed request and orders) should have a very brief handoff by the outgoing resident to the accepting attending; if the patient had admitting orders at the time of the previous handoff the outgoing attending provides the handoff to the accepting attending.

Within 15 minutes of the end of handoff, the accepting resident should assign himself or herself as the resident provider in the FirstNet tracking system.

Within the first 2 hours of the shift, patients that were handed off should have had their chart, laboratory and other findings reviewed and the resident should have physically introduced himself or herself.

Handoff communication guidelines (based on Grice’s Maxims)

Include onlyrelevantinformation.

Be brief.

Beorderly by using the PLAN ED framework.

Behonest. If someone asks a question that you are not 100% sure about (i.e. lab value or result of a scan), find out the answer after the handoff and follow up with the most accurate answer.

by Michael Daignault, MD

Approximately 0.5% of all patient visits to the Emergency Departent (ED) are acute scrotal pain. The differential is long, and includes epidiymitis, orchitis, testicular torsion, torsion of the testicular appendage, testicular trauma, andherniation of abdominal contents into scrotum. In the ED, we are most concerned with testicular torsion, testicular trauma, and herniation. As they say in CVA, time is brain. In this case, TIME IS TESTICLE. This article focuses on evaluation of acute scrotal pain for torsion, as well as the application of bedside ultrasound to evaluate for testicular torsion.

Torsion occurs when the spermatic cord twists around its axis, cutting off vascular flow to the testicle and surrounding structures in the scrotum. Bedside testicular ultrasound can be a very useful adjunct to the history and physical exam in evaluating a patient for torsion. First, IV access should be obtained for laboratory analysis and most importantly to provide analgesia. A urinalysis should also be obtained if possible. Once analgesia is achieved, the patient should be in the supine position with legs spread apart. Ideally the scrotum should be supported with a sling fashioned from a towel and the penis should be covered with a towel that is taped to the abdominal wall (or the patient can be asked to support his penis in a cephalad position). A high-frequency linear ultrasound probe is then applied perpendicular to the penile shaft to obtain transverse view of the scrotum.

In this “saddle view,” both testicles can be viewed in the same window, as in the following picture:

The definitive treatment for torsion is surgery, so in the ED, we are concerned solely with identifying patients who are immediate candidates to go to the OR. As such, on bedside ultrasound, we want to identify patients with a testicle that has decreased or absent blood flow. Change the settings on your ultrasound machine to “doppler” or “color doppler” and first slide the probe while staying in transverse view to the unaffected testicle. You should see multiple pulsations in both red and blue color throughout the testicle signifying vascular flow. It doesn’t matter whether you have more red or more blue. The key is to have a baseline of “normal” vascular flow in your patient so as to compare to the affected testicle.

Next, gently slide the probe (again while staying in transverse view) to the testicle in question. You are looking for a demonstrable reduction or absence in vascular flow compared to the unaffected testicle. In the following image, there is clearly a reduced flow to the right testicle in this patient compared to the left.

Again, bedside ultrasound for testicular torsion should be used as an adjunct to the physical exam and a good history taking. Absence of cremaster reflex remains the most sensitive sign (90-100%) in diagnosing torsion. Complete ultrasound evaluation of the acute scrotum is obviously much more comprehensive than what I have outlined above, but is beyond the scope of both this article and the purview of the emergency physician. However, visualized absence of vascular flow on bedside ultrasound should prompt immediate urology consult and preparation for the OR.

by Michael Daignault, MD

The patient with undifferentiated dyspnea always presents a unique challenge to the emergency physician (EP). That challenge is compounded when that patient becomes unstable or is crashing and the EP cannot quickly identify the problem using traditional available modalities: EMS report, talking to family, initial physical exam, STAT EKG and portable CXR, and the labs are still in progress.

Call it whatever you want – thoracic/chest/lung ultrasound… it has been around for a while, yet EPs are still unfamiliar or daunted by its readily available application to help them with the undifferentiated dyspnea patient. Its use for identifying PE (right heart strain), pneumonia (hepatization of pulmonary parynchema), and tension pneumothorax (lack of lung sliding/stratosphere sign) have been well-described.

Here, I focused on use of lung ultrasound to quickly identify pulmonary edema/acute CHF as a potential cause of dyspnea, focusing on its advantages over traditional modalities.

An all too-common clinical scenario: 60 YO M with PMHx of DM, HTN, COPD/asthma (not on home O2) and ESRD on HD who presented from home with acute dyspnea. EMS noted a very high BP, 220/100. Initial lung auscultation revealed reduced air movement bilaterally (“tight chest”) with scant expiratory wheezing. O2 saturation was 89%. Portable CXR was interpreted as “unremarkable.” Treatments with albuterol/atrovent and IV methylprednisone were stared for presumed COPD/asthma. Patient noted interval improvement, but on reassessment began to acutely decompensate. The resuscitation team was setting up for rapid sequence intubation; thankfully an ultrasound machine was bedside. Using the phased-array “cardiac” probe, the team leader placed visualized something close to this:

With the probe held in place and slightly rocked from side-to-side multiple shimmering lines such of these were seen extending from the pleural line extending all the way down to the bottom of the screen. Known as “b-lines,” they represent interstitial fluid, or pulmonary edema, and are pathological.

To qualify as a B-line, the following criteria should be met:

Extending from the pleural line (the line between 2 ribs as the probe is placed in the intercostals space) all the way down to the bottom of the screen.

There must be a lot of them. There has been many research studies, too numerous to mention here, in attempts to quantify the number of B-lines needed to qualify as pulmonary edema. 1 or 2 B-lines are considered either normal or mild pulmonary edema; what we care about is when there are many lines, too numerous to count. If there are 1-2, and your patient is crashing, odds are that acute pulmonary edema is not the cause.

The B-lines must “erase” physiological A-lines, which are reflections of the pleura line and are seen in a “normal” lung ultrasound here:

The team recognized the aforementioned, applying BiPAP and giving an IV dose of Lasix, with steady improved. By the time the lab tests came back the patient was feeling much better… BNP was >3000 .

This scenario is interesting and common – lung ultrasound was more useful than traditional lung auscultation and CXR, both of which lagged the real-time ultrasound results.

The lesson learned for us was to not wait next time to grab the ultrasound and put the probe on the patient. And secondly, to not use the lung ultrasound as a last resort, but as part of the initial physical exam to quickly differentiate the cause in an acute dyspneic patient.